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重度抑郁症患者杏仁核中的多巴胺能异常:一项尸检研究。

Dopaminergic abnormalities in amygdaloid nuclei in major depression: a postmortem study.

作者信息

Klimek Violetta, Schenck Jane E, Han Hui, Stockmeier Craig A, Ordway Gregory A

机构信息

Department of Psychiatry and Human Behavior, University of Mississippi Medical Center, Jackson 39216, USA.

出版信息

Biol Psychiatry. 2002 Oct 1;52(7):740-8. doi: 10.1016/s0006-3223(02)01383-5.

DOI:10.1016/s0006-3223(02)01383-5
PMID:12372665
Abstract

BACKGROUND

A deficiency of mesolimbic dopamine (DA) is a leading candidate for the etiology of certain symptoms of depression (e.g., anhedonia and loss of motivation). Here we show amounts of dopaminergic proteins in the amygdala, a key brain structure involved in the integration of emotions and stress, in subjects with major depression and in psychiatrically normal control subjects.

METHODS

The specific binding of [(125)I]RTI 55 to the DA transporter, [(3)H]SCH 23390 to the D1 receptor and [(125)I]epidepride to D2/D3 receptors were measured in the right amygdaloid complex in postmortem brains from 11 subjects with major depression and 11 matched control subjects.

RESULTS

The binding of [(125)I]RTI 55 to DA transporter was significantly lower in the basal and central amygdaloid nuclei, whereas the binding of [(125)I]epidepride to D2/D3 receptors was significantly higher in the basal, central, and lateral amygdaloid nuclei in major depression compared with control subjects. No difference in the binding of [(3)H]SCH 23390 to D1 receptors was observed.

CONCLUSIONS

Given that DA depletion in rats can induce a reduction in the DA transporter and an upregulation of D2/D3 receptors, our data are consistent with the hypothesis that major depression is associated with a deficiency of mesolimbic DA.

摘要

背景

中脑边缘多巴胺(DA)缺乏是某些抑郁症状(如快感缺失和动机丧失)病因的主要候选因素。在此,我们展示了重度抑郁症患者和精神正常对照者杏仁核(参与情绪和压力整合的关键脑结构)中多巴胺能蛋白的含量。

方法

在11名重度抑郁症患者和11名匹配对照者的死后大脑右杏仁复合体中,测量了[(125)I]RTI 55与DA转运体、[(3)H]SCH 23390与D1受体以及[(125)I]表哌啶与D2/D3受体的特异性结合。

结果

与对照者相比,重度抑郁症患者基底杏仁核和中央杏仁核中[(125)I]RTI 55与DA转运体的结合显著降低,而基底杏仁核、中央杏仁核和外侧杏仁核中[(125)I]表哌啶与D2/D3受体的结合显著升高。未观察到[(3)H]SCH 23390与D1受体结合的差异。

结论

鉴于大鼠体内DA耗竭可导致DA转运体减少和D2/D3受体上调,我们的数据与重度抑郁症与中脑边缘DA缺乏相关的假设一致。

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